[Clinical evaluation of fibrous and granulomatous mediastinitis].
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Biomedical subjects
Publications and source records attributed to K Morimoto.
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Metabolic activation of benzene by rat liver microsomes and a reduced nicotinamide adenine dinucleotide phosphate-generating system (S-9 mix) induced sister chromatid exchanges (SCEs) and cell division delays in cultured human lymphocytes. There were optimal concentrations of S-9 mix for the conversion of benzene into the active metabolites that exerted these cytotoxic effects. Reduced glutathione prevented the induction of SCEs by benzene plus S-9 mix in a dose-dependent manner. Reduced glutathione (3 mM) also prevented the induction of SCEs by catechol or hydroquinone, active metabolites of benzene and potent inducers of SCEs, strongly suggesting that glutathione did not simply inhibit the activity of S-9 mix to activate benzene but actually prevented the production of DNA lesions by the active metabolites. Pulse treatment of cells with benzene plus S-9 mix produced the largest number of SCEs when administered at 40 hr of culture (fixed at 72 hr) but did not induce SCEs when administered immediately after the beginning of culture. This indicates that induced DNA lesions that could lead to formation of SCEs are removed in time.
This paper reviewed the development of brachytherapy for the past and at present. In Japan, remotely controlled high-dose-rate afterloading intracavitary treatment for uterine cervix carcinoma has become quite common and interstitial radiotherapy with 192Ir hairpin technique for intraoral carsinomas has also been in routine practice at an increased number of institutes in Japan. These has played a great role in eliminating the personnel exposure. Our present efforts are now directed to extend indications to some other cancers, such as bile-duct, pancreas, rectum and prostate. Nearly 20 patients with intraluminal insertion of 192Ir-wire and template technique with 192Ir-wire has just started to apply for rectal had prostate cancer. Permanent implant of 125I has been also of much interest.
We have purified from a membrane fraction of bovine brain a calmodulin-binding protein (calspectin) that shares a number of properties with erythrocyte spectrin: It has a heterodimeric structure with Mr 240 000 and 235 000 and binds to (dimeric form) or crosslinks (tetrameric form) F-actin. We show that calspectin (tetramer) is capable of inducing the polymerization of G-actin to actin filaments by increasing nucleation under conditions where actin alone polymerizes at a much slower rate. Thus, brain calspectin behaves in the same manner as erythrocyte spectrin, supporting the idea that, in conjunction with actin oligomers it comprises the cytoskeletal meshwork underlying the cytoplasmic surface of the nerve cell.
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Norepinephrine (NE) and dopamine (DA) contained in the rat ovary were determined by high-performance liquid chromatography with electrochemical detection. Concentration of ovarian NE reached adult levels around 5 weeks of age, when the first ovulation occurs. During induction of ovulation, the ovarian NE contents increased slightly during the preovulatory phase, followed by a significant decrease in the postovulatory phase, whereas the turnover of ovarian NE decreased during the preovulatory phase. These results suggest that ovarian noradrenergic nerves were in a somewhat inactivated state during the preovulatory phase. Therefore, ovarian sympathetic nerves are considered to participate in mechanisms of the onset of puberty and ovulation.
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The protective effect of sodium selenite (Na2SeO3) against the cytogenetic toxicity of methyl mercury (CH3HgCl) and mercuric chloride (HgCl2) were investigated on human whole-blood cultures in relation to induction of sister-chromatid exchange (SCE). Both mercurials caused a dose-dependent increase in SCEs, methyl mercury being about 5 times more potent than mercuric chloride. Sodium selenite also induced SCEs. However, the simultaneous addition of selenite (1 x 10(-7) -3 x 10(-5) M) to cell cultures containing either methyl mercury (3 x 10(-6) M) or mercuric chloride (1 x 10(-5) M) prevented the induction of SCEs by the mercurial in a clear dose-related manner. When selenite and mercurial were simultaneously added at a molar ratio of 1:2 Na2SeO3:CH3HgCl, or 1:1 Na2SeO3:HgCl2, cells from treated cultures showed no increase in the SCE frequency. These results indicate that selenite and mercury mutually antagonize their ability to cause DNA damage leading to the formation of SCEs. The formation of bis(methylmercuric)selenide, (CH3Hg)2Se, from Na2SeO3 and CH3HgCl, or a high molecular complex consisting of glutathione-Se-Hg from Na2SeO3 and HgCl2 involving the participation of glutathione in RBCs might play a key role in this antagonism between mercury and selenium.
We used a microbioassay to study the distribution of bleomycin in rat brain tumors induced in newborn Sprague-Dawley rats with 1-ethyl-1-nitrosourea (ENU, 50 mg/kg s.c.). Upon suspected successful tumor induction bleomycin (0.1 g/kg i.v.) was administered, and 2 hr later bleomycin concentrations in major organs and tumor tissues were bioassayed using Bacillus subtilis PCI 219 IMC. To determine their histology, the tumors were stained by the immunofluorescence- or immunoperoxidase method using antiserum to astroprotein in addition to the conventional staining methods. There were 11 gliomas each of the brain and spinal cord, 14 schwannomas of the trigeminal nerve and 4 adenomas of the pituitary gland; they developed within 8 (gliomas), 7.3 (schwannomas) and 15 (adenomas) months on average after ENU treatment. The bleomycin concentration and the tumor:plasma concentration ratio were 7.69 +/- 2.84 micrograms/g and 0.13 +/- 0.05 (brain gliomas), 7.10 +/- 3.15 micrograms/g and 0.27 +/- 0.12 (spinal cord gliomas), 5.40 +/- 1.41 micrograms/g and 0.23 +/- 0.05 (schwannomas), 4.83 +/- 1.05 micrograms/g and 0.21 +/- 0.08 (adenomas). Normal brain- and spinal cord tissues scarcely contained bleomycin.
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A nine-year old girl with severe subglottic stenosis secondary to an emergency tracheostomy is presented. Several conservative managements had no significant effect. The patient, however, was successfully extubated by surgical reconstruction with a costal cartilage graft. One year postoperatively, follow up showed no evidence of upper respiratory obstruction or interference with laryngeal growth. Management of severe subglottic stenosis in children is discussed and the usefulness of an autogenous graft for reconstruction of the larynx and upper trachea in the above-mentioned case is documented.
The binding of calmodulin to a brain microsomal fraction rich in synaptic membranes and vesicles was studied using 3H-labeled calmodulin. The binding was Ca2+-dependent and highly specific to calmodulin since it was competitively displaced only by unlabeled calmodulin and not by 200-4,000-fold excess of other proteins that included troponin-C and S-100 protein. Within the physiological pH range, the specific binding, defined as the amount of bound [3H]calmodulin which is displacable by the addition of an excess of unlabeled calmodulin, agreed well with the Ca2+-dependent binding defined as the difference between the total binding in the presence of Ca2+ and the binding obtained with EGTA in place of Ca2+. Both binding activities appeared to be greatest at about pH 7.0. The binding, either specific or Ca2+-dependent, is a calmodulin concentration-dependent saturable process. The dose-dependent curve obtained for increasing concentrations of [3H]calmodulin agreed well with that obtained for mixtures of a fixed concentration of [3H]calmodulin and increasing concentrations of unlabeled calmodulin over the entire concentration range examined. The results serve as the basis for using [3H]calmodulin in binding studies. Scatchard plot analysis of the curve gave two different Kd values for calmodulin, 8.2 X 10(-8) and 5.3 X 10(-7) M. The corresponding maximum binding capacities were 1.0 X 10(14) and 1.6 X 10(14) calmodulin molecules per mg of microsomal protein, respectively. The binding ability of the microsomal fraction was completely abolished by prior treatment with proteolytic enzymes.
The cellular level of AtP and related compounds in ischemic gerbil brain was investigated by high performance liquid chromatography (HPLC). Brain samples were obtained in situ following ligation of the common carotid artery. AMP and ADP peaks in the brain extracts in the ischemic group became much larger whereas the ATP peak decreased dramatically. The most striking finding was an extensive increase of adenosine: 50-100 fold. The levels of inosine and hypoxanthine also increased greatly in typical symptomatic gerbil.